Electroencephalographic Study of the GAB A‐Withdrawal Syndrome in Rats

Abstract

The spatial and temporal EEG features of the epileptogenic syndrome induced by cessation of chronic intracortical GABA infusion in normal rats are described. In the initial stages, the paroxysmal discharges (PDs) induced by withdrawal from unilateral GABA application may appear either unilaterally or bilaterally, although with greater amplitude on the infused side. PDs are transitorily accompanied by behavioral signs of distal myoclonus of the body territory corresponding to the infused area (contralateral hindlimb). Later, the paroxysmal activity becomes more localized, circumscribed to the cannula-infused site and with ipsilateral propagation to anterior cortical areas. The amplitude of PDs decreases progressively while their frequency increases, reaching its maximal value at about 4 h after the first PDs have appeared. In the final stages of the syndrome, which may last several days, clinical manifestations are absent and PDs are activated by slow-wave sleep and reduced during REM sleep and waking. Chronic intracortical applications of taurine failed to induce any electroclinical changes on withdrawal and were unable to inhibit the focus elicited by GABA withdrawal, whereas reinstatement of GABA infusion into the epileptogenic area was effective in blocking the paroxysmal activity. Intracortical infusion of baclofen induced the appearance of an epileptogenic focus that waned on withdrawal. The GABA-withdrawal syndrome appears to be a new model of focal status epilepticus; it may be useful as an experimental model of human partial epilepsy to investigate the role of GABAergic neurotransmission.

Localized transmeningeal muscimol prevents neocortical seizures in rats and nonhuman primates: Therapeutic implications

“…It is worth noting that after washing out muscimol from the epidural cup, withdrawal‐seizures such as those described by Brailowsky et al. (1990) following long‐term cortical GABA infusions, were not observed in any of the described experiments.…”

Network Homeostasis and State Dynamics of Neocortical Sleep

“…However, it is not clear how silencing of the network would downscale synaptic weights and firing rates. According to the homeostatic scaling model (Turrigiano and Nelson, 2004), prolonged silencing of neurons leads to a rebound elevation of spiking (Brailowsky et al 1990). Prolonged network silencing after cortical deafferentation was suggested to be the cause of trauma-induced epileptic excitability (Avramescu and Timofeev, 2008).…”

Iron-induced experimental cortical seizures: Electroencephalographic mapping of seizure spread in the subcortical brain areas

“…13,14 The model thus differs from those focal epilepsy models in which focal epileptiform activity does not become generalized. For example, in the g-aminobutyric acid (GABA)withdrawal focal epilepsy model 35 the epileptogenic process somehow remains localized and limited to the original focus. Our results further showed that, unlike several other generalized cortical seizure models, 36 in the iron-epilepsy model the spike-wave epileptiform activity of the cortical focus is propagated in to the limbic structures.…”